SPID#: 68 The amblyopia that develops in children after the removal of a cataract is particularly difficult to treat and often leads to blindness. The objectives of this project are to understand the neural bases for this and related disorders and, ultimately, to design treatments for amblyopia that are based on sound scientific knowledge. The primary probe used is a neurological defect in motion processing that is linked to loss of binocular function following neonatal deprivation. During the past year, a combination of behavioral, electrophysiological, and neuroanatomical, and physiological optics methods were used to assess these deficits. Findings have demonstrated that motion processing deficits are present even following treatment conditions that give rise to near normal acuity and contrast sensitivity. Thus, treatments for children need to be evaluated in terms of their effects on motion processing as well as on spatial vision. These findings have been presented in abstract form at major scientific meetings, including the Society for Neuroscience and the Association for Research in Vision and Ophthalmology, and have also been published in peer-reviewed journals. Our findings in monkeys can be extrapolated to human infants with aphakic amblyopia, because of the close similarities between this condition as it occurs naturally in humans and experimentally in our monkeys.